Jan 11, 2005

Maternal folate deficiency results in selective upregulation of folate receptors and heterogeneous nuclear ribonucleoprotein-E1 associated with multiple subtle aberrations in fetal tissues

Birth Defects Research. Part A, Clinical and Molecular Teratology
Suhong XiaoAśok C Antony


Homocysteine, which increases in folate deficiency, can upregulate folate receptors (FR) at the translational level by increasing the interaction between a short cis-element in the 5'-untranslated region of FR-alpha mRNA and heterogeneous nuclear ribonucleoprotein-E1 (hnRNP-E1). Perturbation of this RNA-protein interaction on GD8.5 induces neural tube defects and neurocristopathies in mice. FR upregulation can also reduce cell proliferation independently of folate deficiency in some human cells. Accordingly, we tested the hypothesis that sustained murine maternal folate deficiency would negatively impact pregnancy outcomes, upregulate FR, and selectively reduce fetal cell proliferation. Dams were fed chow with various levels of folic acid added for eight weeks before and throughout pregnancy. Following sacrifice on GD17, dams were compared for folate and homocysteine status as well as pregnancy outcomes. Fetuses from some groups were evaluated by specific biochemical, molecular, and immunohistochemical studies for FR, hnRNP-E1, and apoptosis. When compared to dams fed a folate-replete diet, those dams on a folate-depleted diet developed reduced red cell folates and hyperhomocysteinemia and an inverse dose-dependent upregulation...Continue Reading

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Mentioned in this Paper

Fetal Structures
Neural Tube
Untranslated Regions
Entire Diaphragm
Malignant Neoplasm of Spinal Cord
Hormone Receptors, Cell Surface

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Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

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